Response

Sepsis is generally more challenging to identify in cats than it is in dogs.⁸ Dogs classically present with signs similar to those in people: fever, tachypnea, tachycardia, and leukocytosis. Cats are frequently afebrile or hypothermic.⁸ Severe sepsis in cats can result in bradycardia rather than the expected tachycardia. Abdominal pain was a common physical examination finding in cats with severe sepsis but, curiously, not consistent in cats with septic peritonitis.⁵ Although hepatic abscesses are relatively uncommon, some reports describe their clinical features in dogs and cats. Cats with hepatic abscesses are less likely to be febrile, more likely to be hypothermic, and less likely to have increased liver enzyme activities.⁶

Biomarkers. Sepsis biomarkers are an area of active research in human medicine. Several studies have investigated biomarkers in dogs (protein C, endotoxin, tumor necrosis factor, C-reactive protein)^9,15-17; however, there are no studies of biomarkers in clinically septic cats. In an experimental study in which cats were given low-dose endotoxin, rectal temperature increased, blood pressure decreased, and tumor necrosis factor activity and interleukin-6, interleukin-10, and chemokine CXCL-8 concentrations increased.¹⁸ In addition, white blood cell counts decreased and lactate, glucose, creatinine concentrations and prothrombin time increased.

Decreased plasma ionized calcium concentrations are frequently encountered in people with sepsis and have also been documented in septic cats.^5,21 Etiologies identified in people include parathyroid gland suppression, inadequate vitamin D concentrations, and parathyroid hormone-vitamin D resistance, but the cause of these changes in patients with sepsis is still unknown.

The general pattern of glucose derangements in patients with acute sepsis consists of early and transient hyperglycemia followed by hypoglycemia. Cats are known to become hyperglycemic in response to stress, but hypoglycemia is often seen in septic cats.⁸ The factors thought to play a role in the development of hypoglycemia include increased peripheral glucose utilization, impaired gluconeogenesis, and depleted glycogen stores.

In cats with severe sepsis, hypoalbuminemia is common.⁵ The exact cause is unknown, but hepatic dysfunction, malnutrition, and the shifting of protein production from albumin to acute phase proteins all likely contribute. Hepatic dysfunction can be a serious sequela of sepsis. Blood supply to the liver is impaired in septic shock, resulting in a decrease in oxygen and nutrient delivery. Hepatic dysfunction can result in coagulopathies, mental depression, hypoalbuminemia, and hypoglycemia. Septic cats often have elevated serum bilirubin,^5,8 so they may be overtly icteric on physical examination. Red blood cell lysis, sepsis-induced cholestasis, and hepatic dysfunction are thought to contribute to the development of hyperbilirubinemia in these cats.

Organ dysfunction

The lungs are often considered the shock organ in cats. As such, septic cats may be particularly susceptible to fluid overload, and pulmonary edema and pleural effusion are common. This pulmonary compromise occurs because of increased vascular permeability, sepsis-induced myocardial dysfunction, and decreased colloid oncotic pressure due to hypoalbuminemia. That differs from dogs, in which the liver and gastrointestinal tract are the primary shock organs.

DIAGNOSTIC TESTS

Initial diagnostic tests in cases of septic cats generally consist of a complete blood count, a serum chemistry profile, a urinalysis and culture, thoracic and abdominal radiography, and abdominal ultrasonography. Additional diagnostic tests may include blood bacterial cultures, an endotracheal wash and culture, echocardiography, a cerebrospinal fluid tap, or diagnostic peritoneal lavage.